作者: Francisca Nathalia de Luna Vitorino , Fabio Montoni , Jaqueline Neves Moreno , Bruno Ferreira de Souza , Mariana de Camargo Lopes
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摘要: Fibroblast growth factor 2 (FGF2) is a well-known cell proliferation promoter; however, it can also induce cycle arrest. To gain insight into the molecular mechanisms of this antiproliferative effect, for first time, early systemic proteomic differences induced by in K-Ras-driven mouse tumor line using quantitative proteomics approach are investigated. More than 2900 proteins quantified, indicating that terms associated with metabolism, RNA processing, replication, and transcription enriched among differentially expressed upon FGF2 stimulation. Proteomic trend dynamics indicate that, mainly DNA replication carbohydrate an stimulus delays their abundance changes, whereas stimulation accelerates other metabolic programs. Transcription regulatory network analysis indicates master regulators stimulation, including two critical factors, FOSB JUNB. Their expression dynamics, both Y1 (a murine model adenocarcinoma cells) human lines (SK-N-MC UM-UC-3) susceptible to effects, Both protein levels depend on fibroblast receptor (FGFR) src signaling. JUNB knockdown do not rescue cells from arrest FGF2; delay, underlies one namely, S-phase progression delay.